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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Compared to control subjects, patients with essential hypertension (EH) had a decreased urinary DA:NE ratio and an overall increase in the total (free + sulfated) plasma sum of NE, E and DA. With age-matching, this elevation was found to be due to augmented levels of DA sulfate. When subdivided into borderline (labile) and stable EH groups, only the borderline EH patients had heightened plasma DA sulfate levels, enhanced urinary homovanillic acid excretion and tended to have plasma NE and PRA increases. Patients with stable EH had a hyporesponsive urinary DA and Na+ excretion as well as reduced PRA levels at the height of furosemide-induced natriuresis. These data are compatible with a hyperdopaminergic component of the hyperadrenergic state, more or less affecting patients with borderline EH in contrast to the hypodopaminergic features of subjects evolving into stable EH in whom the neurogenic component subsides. In both EH subgroups, urinary DA lagged behind NE excretion. Dopaminergic tone may indirectly affect endogenous DA-modulated renal, adrenal and vascular synaptic processes as well as their responses to exogenous Angiotensin II and DA, respectively.
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PMID:The heterogeneity of dopamine involvement in essential hypertension. 266 48

To evaluate the activity of sympathetic system and of plasm renin in elderly patients with borderline (BH) and established essential hypertension (EH), 31 BH mean age 38 years and 30 EH, mean age 39 years; 15 BH, mean age 66 years, and 15 EH, mean age 68 years, were studied at rest and after dynamic exercise. At the same time blood pressure and heart rate were automatically recorded, while blood samples were collected for PRA and plasma epinephrine (E) and norepinephrine (NE) assays. Plasma E levels showed no significant differences between the groups examined at rest. Nevertheless, young BH had higher plasma E levels than young EH after stress and elderly BH showed plasma E levels higher than age-matched EH in response to dynamic exercise. The PRA behaviour was similar among all the groups, but dynamic exercise induced a greater increase in BH than in EH. Moreover, the stress-induced increase in plasma NE levels was higher in EH than in BH. Our results demonstrate in old BH, as well as in young BH, a response of E to stress greater than in the age-matched EH. In our study BH, both young and old subjects, seem to be characterized by a sympathoadrenal overactivity pointed out by an excessive release of E from the adrenal gland after stress. This exaggerated sympathoadrenal reactivity may constitute an important mechanism in triggering hypertension independent of age.
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PMID:Epinephrine and norepinephrine pattern in elderly patients with borderline and established hypertension. 266 50

Patients with untreated essential hypertension had significantly higher plasma atrial natriuretic factor (ANF) levels (92.9 +/- 12.9 pg/ml, mean +/- SE) than those of age-matched controls (37.8 +/- 6.0 pg/ml; p less than 0.01). Plasma ANF levels in essential hypertensive patients showed a significant positive correlation with mean arterial pressure (MAP; r = 0.46, p less than 0.05) and an inverse correlation with plasma renin activity (PRA; r = -0.43, p less than 0.05). Plasma ANF levels after medication showed significant correlation with the decrease in MAP (r = 0.565, p less than 0.05). Patients with primary aldosteronism had significantly higher plasma ANF levels (122.4 +/- 30.2 pg/ml, n = 8) than those of controls (p less than 0.05). The levels returned to normal after extirpation of adrenal tumors. The response of plasma ANF levels in patients with primary aldosteronism to volume expansion with infusion of 2 L of physiological saline in 2 hours was greater than in controls. Such exaggerated response disappeared after surgical treatment. Infusion of angiotensin II (Ang II; 20 ng/kg/min) or norepinephrine (200 ng/kg/min) for 30 minutes to normal volunteers (n = 5) resulted in a rise in MAP (24.9 +/- 3.3 and 15.8 +/- 4.4 mm Hg, respectively) and a twofold increase in plasma ANF level. Infusion of the Ang II antagonist [Sar1, Ile8]Ang II (600 ng/kg/min) for 30 minutes, resulted in a rise in MAP (18.8 +/- 2.1 mm Hg) and more than a twofold increase in plasma ANF level in patients with essential hypertension (n = 6).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Atrial natriuretic factor in essential hypertension and adrenal disorders. 296 1

The antihypertensive effect of a non-sulfhydryl, long acting ACE (angiotensin converting enzyme) inhibitor, MK-421, was evaluated by administering a single dose of 10 mg to 13 patients with mild to moderate essential hypertension. The pharmacokinetic profile of MK-421 and its potent active metabolite, MK-422, was also assessed, together with the effect on the various components of the renin-angiotensin system. A single dose of MK-421 produced a significant fall in MBP from 2 to 24 hours post-drug. As could be expected, plasma ACE activity was suppressed up to 24 hours after MK-421. The half-life of MK-422, Cmax and [AUC]24(0) of MK-421 and MK-422 were measured. No significant change in plasma bradykinin or urinary excretion rate of kallikrein was observed, whereas a slight increase was observed in the urinary excretion rate of kinins after MK-421 in 8 patients. Significant correlations were observed between pretreatment PRA levels and the maximum fall in MBP.
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PMID:Serum concentration and effects of a single dose of enalapril maleate in patients with essential hypertension. 298 51

To assess if dopaminergic control of aldosterone secretion is mediated by the renin-angiotensin system, the effect of chronic angiotensin converting enzyme inhibition by enalapril on the aldosterone response to metoclopramide has been studied in 10 patients with mild to moderate essential hypertension. Enalapril reduced supine blood pressure and increased the heart rate significantly. Plasma renin activity and urinary sodium excretion rose significantly. PRA was not changed by metoclopramide, neither during placebo nor during enalapril treatment. Metoclopramide induced a two-fold increase in plasma aldosterone, the peak response being reached within 15 min. Enalapril treatment did not alter the aldosterone response to metoclopramide. Dopaminergic control of aldosterone secretion appears to be independent of the renin-angiotensin system.
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PMID:Stimulation of aldosterone secretion by metoclopramide is not affected by chronic converting enzyme inhibition. 300 Jul 95

The present study was designed to clarify the role of serum angiotensin I-converting enzyme (ACE) in the occurrence and maintenance of hypertension in essential hypertension (EH). For this purpose, following experiments were carried out: 1) Correlations between serum ACE activity and renin activity (PRA), aldosterone concentration (PAC) and bradykinin concentration (PBC) in plasma, and blood pressure (BP) as well as serum creatinine levels. 2) Circadian rhythm of serum ACE activity. and 3) Effect of furosemide, upright posture, both furosemide and upright posture, propranolol, indomethacin, 9 alpha-fluorocortisol or angiotensin II (A-II) on the serum ACE activity, PRA, PAC and circulating plasma volume (CPV). The following results were obtained: The serum ACE activity was 30.2 +/- 5.0 U/ml (means +/- SD) in EH as a group, which was significantly higher than that (27.3 +/- 3.9 U/ml) in age matched normotensive subjects (NT) (p less than 0.001). While there was no significant difference in the enzyme activity between low-renin EH (LREH) and NT, a significant difference was found between normal- (NREH) or high-renin EH (NREH) and NT (p less than 0.05 for NREH, p less than 0.01 for HREH). A negative correlation was observed between enzyme activity and age in EH (r = -0.221, 0.05 less than p less than 0.10) as well as in NT (r = -0.306, p less than 0.05). No significant relationships were observed between enzyme activity and BP in either EH or NT. There was a significant positive correlation between enzyme activity and PRA in NT. (r = 0.501, p less than 0.001), NREH (r = 0.658, p less than 0.001) and HREH (r = 0.695, p less than 0.001). However, no significant relationship was found between them in LREH. The enzyme activity was significantly correlated to PAC in NT (r = 0.368, p less than 0.01), NREH (r = 0.567, p less than 0.001) and HREH (r = 0.529, p less than 0.01), but not in LREH. Although no significant correlation was observed between enzyme activity and PBC in NT, NREH and HREH, a significant relationship was found in LREH (r = -0.460, 0.05 less than p less than 0.10). The enzyme activity was not related to serum creatinine levels in EH as well as in NT. In NT, the serum levels of ACE activity reached a maximum values at 6:00 a.m. or 9:00 a.m., and gradually decreased between 6:00 p.m. and 3:00 a.m. An almost similar circadian rhythm of enzyme activity was found in EH.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Clinical significance of serum angiotensin I-converting enzyme in essential hypertension]. 300 63

In 12 patients with essential hypertension who remained hypertensive despite chronic chlorthalidone treatment, the effect of 2 weeks of additional therapy with the converting enzyme inhibitor (CEI) enalapril on blood pressure and body fluid volumes has been evaluated. The objective was to examine the influence of a diuretic-stimulated renin-angiotensin-aldosterone system (RAAS) on haemodynamics and body fluid volume. Mean arterial pressure (MAP -21%), total peripheral resistance index (TPRI -22%) and plasma aldosterone concentration (PAC -39%) were decreased, and plasma renin activity (PRA 660%) was increased. The average heart rate (HR), cardiac index (CI), plasma volume (PV), blood volume (BV), extracellular fluid volume (ECFV) and body weight (BW) remained unchanged. A negative correlation was found between the per cent changes in ECFV and PAC. Thus, body fluid volumes during chronic diuretic treatment are well preserved even when the RAAS with its sodium retaining properties is suppressed by CEI. Possible mechanisms are a volume (not angiotensin II) - dependent stimulation of aldosterone and a fall in blood pressure.
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PMID:Changes in haemodynamics and body fluid volume due to enalapril in patients with essential hypertension on chronic diuretic therapy. 302 15

The effect of chronic converting enzyme inhibition with enalapril on the PRA, PRL and plasma aldosterone responses to metoclopramide was studied in 10 patients with mild to moderate essential hypertension. Enalapril reduced supine blood pressure and increased heart rate significantly. PRA and urinary sodium excretion rose significantly. PRA levels did not change after metoclopramide neither during placebo nor during enalapril. The aldosterone response to metoclopramide was not altered by enalapril, indicating that this response is independent of the renin-angiotensin system. The PRL response to metoclopramide was considerably enhanced after 4 weeks of treatment with enalapril. It is proposed that enalapril, by decreasing the formation of angiotensin II, increases the prolactin reserve.
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PMID:Enhanced response of plasma prolactin to metoclopramide during chronic converting enzyme inhibition. 303 57

The purpose of the study was to characterize the renal TxA2, PGI2 and PGF2 alpha release in response to arterial blood pressure (BP) fall induced by systemic and intrarenal vasorelaxation in subjects with essential hypertension. Significantly enhanced TxB2- and PGF2 alpha excretion and no change in ratio TxB2/6-keto-PGF1 alpha were found in urine in hypertensive patients after administration of the Ca++ entry blocker gallopamil, used to induce BP fall. This response was associated with significant PRA elevation in peripheral venous samples. In in vitro experiments, direct and indirect effects of gallopamil on renal tissue could be distinguished. Gallopamil resulted in significant diminution of TxA2 production and a decrease in TxB2/6-keto PGF1 alpha ratio in incubated rat kidney slices. This model was also used to test biochemically the effect of reflex sympathetic activation on prostanoid generation in kidney. It was concluded that this mechanism was only one among the indirect mechanisms by which gallopamil could induce that renal prostanoid response in hypertensive subjects. The response in urinary TxB2- and PGF2 alpha excretion was found to be significantly related to the changes in sodium reabsorption. These results suggested, that the increase in renal TxA2 and PGF2 alpha production in response to systemic and intrarenal "vasodilation" induced by gallopamil in hypertensive subjects can be interpreted as part of counteraction of the kidneys to BP fall.
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PMID:Prostanoid response in the kidney of hypertensive subjects as part of renal counteraction to gallopamil-induced blood pressure decrease. 307 78

Using pulsed Doppler methods, hemodynamics of the common carotid and the brachial arteries were measured in 10 patients with essential hypertension. After vasodilatation due to Cadralazine, a Dihydralazine-like substance, mean arterial pressure significantly decreased and heart rate increased. Change in PRA was significantly and positively correlated with the change in heart rate. In the brachial artery circulation, diameter and vascular resistance decreased while blood flow velocity and volumic blood flow did not increase significantly. In the common carotid artery circulation, diameter, mean blood flow did not change. However, vascular resistance and tangential tension decreased slightly. The increase in heart rate was strongly and negatively correlated (r = 0.82 p less than 0.01) with the change in the carotid artery tangential tension (measured as the product between mean arterial pressure and arterial radius) while no comparable correlation was observed with the change in blood pressure or arterial radius alone. The study suggested that in essential hypertensives, modifications in the carotid artery tangential tension secondary to arteriolar vasodilatation contribute actively to the baroreflex response.
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PMID:[Non-invasive study of the role of carotid distension in the baroreflex response to the arteriolar vasodilator cadralazine in essential hypertension]. 309 14


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